Results 71 to 80 of about 208,684 (264)

Metastasis on pause: How dormant tumor cells stay hidden within the tumor microenvironment and evade immune surveillance

Molecular Oncology, EarlyView.
Dormant cancer cells can hide in distant organs for years, evading treatment and the immune system. This review highlights how signals from the surrounding tissue and immune environment keep these cells inactive or trigger their reawakening. Understanding these mechanisms may help develop therapies to eliminate or control dormant cells and prevent ...
Kanishka Tiwary, Jose Javier Bravo‐Cordero   +1 more
wiley   +1 more source

Breast neoplasm epithelial-mesenchymal transition and cytokines: a systematic review

Cancer Cell International
A crucial aspect of the association involving inflammation and the development of cancer is the ability of cancer cells to undergo a transition into mesenchymal cells. The process is referred to as epithelial-mesenchymal transition (EMT).
Yian Chen, Haining Ding, Jiaqing Song, Xiufei Gao   +3 more
doaj   +1 more source

An angiotensin system inhibitor (losartan) potentiates antitumor efficacy of cisplatin in a murine model of non–small cell lung cancerCentral MessagePerspective

JTCVS Open
Objective: Previous studies have demonstrated synergistic antitumor effects of angiotensin system inhibition (ASI) combined with cisplatin therapy in pancreatic cancer.
Hexiao Tang, MD, PhD, Eric Abston, MD, PhD, Mozhdeh Sojoodi, PhD, Yongtao Wang, PhD, Derek J. Erstad, MD, Zenan Lin, MD, Bryan C. Fuchs, PhD, Kenneth K. Tanabe, MD, Michael Lanuti, MD   +8 more
doaj   +1 more source

Loss of IGF‐1R impairs DNA‐PKcs recruitment to chromatin leading to defective end‐joining

Molecular Oncology, EarlyView.
IGF‐1R promotes radioresistance by facilitating DNA‐PKcs recruitment to chromatin, enabling non‐homologous end‐joining (NHEJ) repair of double‐strand breaks. Inhibition or loss of IGF‐1R disrupts this recruitment to damage sites, driving compensatory reliance on microhomology‐mediated end‐joining (MMEJ) repair.
Matthew O. Ellis, Jack V. Mills, Wojciech Niedzwiedz, Valentine M. Macaulay   +3 more
wiley   +1 more source

Flow Enabled Target Capture Halbach‐based magnetic enrichment increases circulating tumor cell capture from blood in metastatic cancer patients

Molecular Oncology, EarlyView.
Pair‐wise comparison of the CellSearch and FETCH enrichment technologies for circulating tumor cells (CTCs) from metastatic breast, prostate, and small cell lung cancer patients shows an increased capture of CTCs using FETCH enrichment. The clinical implementation of circulating tumor cells (CTCs) as a predictive tool for therapy efficacy in the ...
Michiel Stevens, Anouk Mentink, Tom Niessink, Frank Coumans, Leonie Mekenkamp, Ruchi Bansal, Jeroen Hiltermann   +6 more
wiley   +1 more source

Epithelial–Mesenchymal Transition in Acute Leukemias

International Journal of Molecular Sciences
Epithelial–mesenchymal transition (EMT) is a metabolic process that confers phenotypic flexibility to cells and the ability to adapt to new functions. This transition is critical during embryogenesis and is required for the differentiation of many tissues and organs.
Lokman Varisli, Spiros Vlahopoulos
openaire   +4 more sources

UBR5 regulates the progression of colorectal cancer cells through Snail-induced epithelial–mesenchymal transition

Genes and Diseases
Snail is a core inducer of epithelial-to-mesenchymal transition. Here, we show that UBR5 promotes ubiquitin-mediated degradation of Snail and regulates the progression of colorectal cancer cells through its E3 ubiquitin ligase function. UBR5 specifically
Xinyue Zhao, Ruiying Liu, Zhihui Han, Zehao Li, Ling Mei, Yuyang Liu, Xueqi Fu, Yue Jin   +7 more
doaj   +1 more source

USP29‐regulated noncanonical stabilization of the hypoxia‐inducible factor‐α in aggressive prostate cancer

Molecular Oncology, EarlyView.
We identify USP29 as the only DUB mirroring CA9 expression, a marker of hypoxia and HIF pathway activation associated with PCA aggressiveness. USP29 stabilizes HIF‐1α and HIF‐2α via a noncanonical mechanism that is independent of PHD/pVHL activity yet relies on proteasomal regulation, establishing USP29 as a previously unrecognized regulator of hypoxic
Amelie S Schober, Leire Moreno‐Cugnon, Laura Martínez‐Pérez, Amaia Ercilla, Amaia Zabala‐Letona, Adrián Vicente‐Barrueco, Maider Fagoaga‐Eugui, Saioa Garcia‐Longarte, Blanca Calle‐Ciborro, Encarnación Pérez‐Andrés, Onintza Carlevaris, Sara Pozo, Isabel Mendizabal, Ugo Mayor, Arkaitz Carracedo, Violaine Sée, Edurne Berra   +16 more
wiley   +1 more source

Epithelial-mesenchymal transition in liver fibrosis

Biomedical Reports, 2016
Liver fibrosis is the result of a sustained wound healing response to sustained chronic liver injury, which includes viral, alcoholic and autoimmune hepatitis. Hepatic regeneration is the dominant outcome of liver damage. The outcomes of successful repair are the replacement of dead epithelial cells with healthy epithelial cells, and reconstruction of ...
Ya-Lei, Zhao, Rong-Tao, Zhu, Yu-Ling, Sun   +2 more
openaire   +3 more sources

Oncogenic DMTF1β promotes cancer cell motility by regulating autophagy through ULK1 stabilization

Molecular Oncology, EarlyView.
In the current study, we demonstrate that the oncogene DMTF1β regulates ULK1 stability by reducing its proteasomal degradation in cancer cells. This stabilization enables ULK1 to induce autophagy, which in turn facilitates cancer cell migration. Consequently, reduced DMTF1β levels lead to decreased autophagy and impaired cancer cell migration.
Jun Xu, Nicolas J. Niklaus, Anna M. Schläfli, Igor Tokarchuk, Magali Humbert, Federico La Manna, Bich Vu, David Maul, Ramin Radpour, Marianna Kruithof‐de Julio, Inti Zlobec, Jörn Dengjel, Bruce E. Torbett, Mario P. Tschan   +13 more
wiley   +1 more source